DESCRIPTION (Adapted form the applicant's abstract): The investigators plan to study 16 patients with early PD, 16 controls who are spouses, and 16 unrelated age and sex-matched controls. Patients and controls will undergo platelepheresis in order to collect mitochondria for study. The patients will be studied prior to drug therapy, after 1 month of treatment with carbidopa/L-dopa, after two years of drug treatment. Mitochondria studied in a blind fashion will undergo extensive evaluation of the electron transport chain and western blotting studies. This work will confirm or refute earlier published work suggesting platelet mitochondrial complex I deficiency in PD, study the effects of the 2 most commonly used therapies on mitochondrial function and longitudinally evaluate effects of two years of disease progression on platelet mitochondrial electron transport activities and immunologically active complex III. As effective therapies to slow the course of the disease are now available, it is important to establish the significance of electron transport deficiencies in PD. Such studies might confirm a biological marker which will provide insight into the etiology of PD and might be used to confirm early PD and possibly identify at-risk patients.